Enzimas pancreáticas: revisión y análisis de sus acciones atenuantes sobre la secreción ácida gástrica, el dolor pancreático, el colon irritable y trastornos digestivos múltiples / Pancreatic Enzymes: useful therapeutical agents to a wider spectrum of functional digestive disorders. Revision and analysis

Las enzimas pancreáticas constituyen agentes terapéuticos de utilidad clínica dentro de un espectro mucho más amplio del que se acepta habitualmente. En este trabajo se trata de demostrar que ejercen una influencia benéfica en un variado grupo de entidades... y que la asociación de una mejora en el mecanismo del proceso digestivo, especialmente de los carbohidratos, y el consecutivo alivio de los fenómenos dispépticos fermentativos, ello en conjunción con una atenuación de la hipersensibilidad del sistema nervioso aferente, cambio muy ligado a una depresión liberadora sobre la CCK, explican el valor terapéutico innegable que poseen los fermentos pancreáticos en el enfoque terapéutico del colon irritable

COX-2, NSAIDs and human neoplasia. Part I: Colorectal neoplasms.

Cyclooxygenase-2 (COX-2), the inducible cyclooxygenase isozyme involved in the conversion of arachidonic acid (AA) to biologically active prostanoids, has become the subject of intense interest during the last few years. The recent surge of interest stems from seminal studies that correlated elevated expression of COX-2 with tumor induction and progression, and epidemiological studies that correlated reduced risk of developing certain types of cancers with chronic use of non-steroidal anti-inflammatory agents (NSAIDs). Although these observations were first reported with colorectal cancer (CRC), similar findings have subsequently been made with other types of cancers. A wide spectrum of studies continue to be undertaken in both laboratory and clinical settings to elucidate the mechanisms underlying these anti-tumor effects of COX-2 for potential translation into cancer chemoprevention and therapy. The aim of this article is to present a review of COX genes, the prostaglandin-cyclooxygenase relationship, the role of COX-2 in carcinogenesis and the rationale for targeting COX-2 with NSAIDs for cancer chemoprevention. Special emphasis is given to the role of COX-2 expression in the genesis and progression of colorectal neoplasia, and its correlation with other pathological characteristics of CRC. Preliminary observations on COX-2 expression in inflammatory bowel disease (IBD)-related colorectal neoplasia are also presented.

[The role of monoamine oxidase in large intestine pathology]. / Rol' monoaminoksidazy v patologii tolstoi kishki.

The activity of monoamine oxidase (MAO) was studied during functional, inflammatory and tumoral diseases of the large intestine. In the patients with the irritable colon syndrome, the enzymatic activity was decreased by 34% at the acute stage of the disease and in those with nonspecific ulcerative colitis it was increased by 44%. Follow-ups of MAO activity may serve as an indicator of the adequacy and efficiency of the treatment performed.

Clinical relevance of lysozyme in the faeces.

To elucidate the value of faecal lysozyme determination in the differential diagnosis of patients with atypical abdominal complaints, stool samples of healthy controls, patients with irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) were analysed. Faecal lysozyme concentration in healthy controls ranged from 0 to 6 mg/l with a mean of 3 mg/l. Patients with IBS had similar faecal lysozyme levels. In contrast, faecal lysozyme concentrations in patients with IBD were increased (range 6 to 104 mg/l). The difference between patients with IBS and IBD was highly significant (P less than 0.001). The determination of faecal lysozyme concentration may provide a useful test in the work-up of patients with abdominal complaints. In addition, the faeces lysozyme concentration appeared to be an objective parameter of the inflammatory activity of IBD in 11 patients investigated.

Faecal lysozyme: determination, reference intervals and some data in gastro-intestinal disease.

After diluting faecal samples with a solution of Brij and saline and subsequently ultrafiltrating the faecal mixtures, lysozyme concentration can be reproducibly measured in the obtained faecal fluids, using a turbidimetric method. Measuring faecal lysozyme concentration enables discrimination normal individuals and patients with irritable bowel syndrome between patients with inflammatory bowel disease and colonic cancer. Lysozyme distribution in stools appears to be homogeneous. Faecal lysozyme concentration is stable when samples are stored during at least 1 wk at 6 degrees C. It appears that the lysozyme activity is directly correlated with the clinical status and severity of the disease. Faecal lysozyme may thus serve as an important tool both in diagnosis and in follow-up in the out-patients clinic for gastroenterology.

[New results in the diagnosis and therapy of functional disorders of the large intestine]. / Neue Ergebnisse in Diagnostik und Therapie der funktionellen Störungen des Dickdarmes.

The most important pathophysiological mechanism of functional disorders of colon is motility disturbance. The best term for these disturbances is considered to be "colon dyskinesia". Dyskinesia can be classified as primary and secondary, and as hyperand hypokinetic. The following clinical forms are distinguished: with constipation, painless diarrhea, isolated pain syndrome, colica mucosa. Inflammatory diseases of colon are accompanied by chemical changes in feaces: the increase of enterokinase and alkalien phosphatase activity (enzymorrhea), the increase of feacal excretion of protein (proteinorrhea). Both enzymorrhea and proteinorrhea are absent in colon dyskinesia. The investigation of enzymes and protein in faeces can be of great help in differential diagnostics of functional and inflammatory colon diseases. In treating colon dyskinesia psychopharmacological, cholinolytical, spasmolytical and antidiarrrheal preparations are used, as well as some drugs with purgative effect. Clinical and instrumental methods make it possible to determine which type of the motility disturbances predominates. The latter is important for differential prescription of drugs correcting colon motility in colon dyskinesia. Colon motility in man ist actively affected by adrenergic drugs: it is inhibited by adrenomimetics and stimulated by adrenolytics which justifies their prescription in colon dyskinesia. Diazepam and phenobarbital inhibit colon motility. Diphenoxylate and metoclopramide have a normalizing effect.

Irritable bowel syndrome. Role of lactase deficiency.

In adults with the irritable bowel syndrome who had no history of milk intolerance, the prevalence of lactase deficiency and the value of lactose restriction were determined. Eighty subjects with the irritable bowel syndrome who were white, non-Jewish, and of northern-western European background were screened for lactase deficiency by means of the hydrogen breath test. Lactase deficiency was found in 5 of the 80 subjects with the irritable bowel syndrome and in 6 of the 100 subjects without intestinal symptoms who were of comparable ethnic background. After exclusion of milk from the diet, three of the five subjects with lactase deficiency and the irritable bowel syndrome had partial to complete relief of symptoms for 3 weeks, and two of these had sustained relief for 1 year (one with complete and one with 75% improvement). Lactase deficiency was found to be a relatively uncommon cause of irritable bowel symptoms among non-Jewish whites who are of northern-western European background.

Determination of prostaglandin synthetase activity in rectal biopsy material and its significance in colonic disease.

A method is described for determining prostaglandin synthetase activity in milligram amounts of tissue. The procedure is based on the conversion of 14C-arachidonic acid to prostaglandin E2 and F2alpha-like substances. High levels of prostaglandin synthetase activity occurred in the inflamed mucosa of patients with ulcerative colitis and fell during successful drug therapy, but it is not yet known whether the cause of the inflammation first involves increased PG synthetase activity, or whether inflammation caused increase of PG synthetase.

Prolyl hydroxylase activity in serum and rectal mucosa in inflammatory bowel disease.

Prolyl hydroxylase activity in rectal mucosa was found to be significantly greater in 11 patients with Crohn's disease than in 11 control subjects with the irritable bowel syndrome and 16 patients with ulcerative colitis (P less than 0.005). Seven of the patients with Crohn's disease had a histologically normal rectum. This abnormality in apparently normal mucosa supports the concept that Crohn's disease is a 'continuous' disease of the gastrointestinal tract. Although there was no significant difference in prolyl hydroxylase activity between control subjects and patients with ulcerative colitis, those patients with quiescent disease tended to have lower values than those with active mucosal inflammation. Prolyl hydroxylase activity could not, however, be detected in the sera of either healthy control subjects or patients with inflammatory bowel disease.

Abnormalities in the apparently normal bowel mucosa in Crohn's disease.

The uninvolved intestinal mucosa away from the affected areas in Crohn's disease has always been considered to be macroscopically and microscopically normal. Rectal biopsy specimens from 13 patients who had had Crohn's, disease elsewhere in the bowel, but never in the rectum, showed significant increases in the plasma-cell density in the lamina propria, in the volume of the lamina propria, and in the glucosamine-synthetase activity of the specimens, compared with a control series of patients with the irritable-colon syndrome. It is suggested that the colonic mucosa is always abnormal in Crohn's disease even if macroscopical and histological examination shows an apparently normal mucosa.

Dipeptidase deficiency and malabsorption of glycylglycine in disease states.

The activities of jejunal mucosal peptide hydrolases for glycylglycine, glycyl-L-leucine and L-leucylglycine, were assayed in 37 patients. Eight patients, four of whom had Crohn's disease, were found to have a marked reduction in the activity of glycylglycine dipeptidase and, to a lesser extent, of the other two hydrolases. Although absorption of glycine in the two groups was similar, there was malabsorption of glycylglycine in the patients with reduced dipeptidases as shown by a flat absorption curve. The importance of peptide hydrolases of small-intestinal mucosa in the final digestion of proteins, and the implications of peptidase deficiency in disease states is discussed. It is concluded that significant peptidase deficiency may occur even when the mucosa is otherwise histologically completely normal, similar to some states of disaccharidase deficiency described in recent years.